New strains of community-acquired methicillin-resistant Staphylococcus aureus with Panton–Valentine leukocidin causing an outbreak of severe soft tissue infection in a football team

Abstract

A new category of methicillin-resistant Staphylococcus aureus (MRSA), designated community-acquired MRSA (CA-MRSA), has been noted increasingly in the community in the past 14 years [1]. CA-MRSA strains have different genetic backgrounds than hospital-acquired MRSA, as evidenced by pulsed-field gel electrophoresis (PFGE) patterns, and thus do not descend from nosocomial strains. They also carry a novel staphylococcal cassette chromosome (SCC) mec type IV element, which is differentiated from the hospital-acquired MRSA SCCmec types I-III by its smaller size and the absence of non-s-lactam genetic resistance determinants. In addition, CA-MRSA strains replicate more rapidly than hospital-acquired MRSA strains, they have a better ability to colonize humans, and they possess genes for different toxins [2]. Major risk factors for CA-MRSA colonization, as recognized by Ellis et al. [3], are treatment with systemic antibiotics and skin trauma. The strains producing Panton–Valentine leukocidin cause furunculosis and severe necrotic hemorrhagic pneumonia in otherwise healthy individuals [3, 4]. Outbreaks have been described in day-care and athletic settings. Sport teams are especially vulnerable to infections with these strains because of frequent skin trauma and close contact of team members [4]. In order to detect outbreaks of new CAMRSA, molecular typing [5–8] should be performed and virulence genes detected [9]. Reported here is an outbreak of severe soft tissue infection affecting a football team, which was caused by a new strain of community-acquired methicillin-resistant Staphylococcus aureus carrying the Panton–Valentine leukocidin gene. From July to October 2004, a football team consisting of 26 members (24 players, a coach and a masseur, all male) was affected by a severe, highly transmissible CA-MRSA soft tissue infection. In order to diagnose the infection and investigate the genetic background and virulence of the involved strains, we studied 246 specimens obtained from the team members’ furuncles, skin and nasal surveillance cultures and postoperative wounds. Specimens were plated onto blood agar and oxacillin resistance screening agar base (ORSAB) medium. Isolates were identified as S. aureus by their growth as yellow colonies, with or without hemolysis on blood agar and by the results of Gram staining, catalase, DNase test and tube coagulase test. Blue-colored colonies that appeared after 2 or 3 days of incubation on ORSABmedium were suspected of being possible MRSA. Susceptibility testing was performed using the Kirby–Bauer disk diffusion method, as recommended by the Clinical and Laboratory Standards Institute (formerly NCCLS) [10]. Methicillin resistance was determined using the 1 μg oxacillin disk method and confirmed by oxacillin plate (Mueller–Hinton agar containing 4% NaCl and 6 μg/ml oxacillin), cefoxitin disk and Etest methods. Susceptibility to penicillin, erythromycin, clindamycin, trimethoprim/sulfamethoxazole, vancomycin, rifampin, gentamicin, ciprofloxacin, teicoplanin, linezolid, mupirocin and fusidic acid was determined. Oxacillin resistance was confirmed by the simultaneous detection of M. Muller-Premru (*) . K. Seme . N. S. Kucina . V. Spik . M. Gubina Institute of Microbiology and Immunology, Medical Faculty, Zaloska 4, Ljubljana, Slovenia e-mail: manica.mueller-premru@mf.uni-lj.si Tel.: +386-1-5437425 Fax: +386-1-5437401